Mitochondrial reactive oxygen species modulate mosquito susceptibility to Plasmodium infection |
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Authors: | Renata L S Gonçalves Jose Henrique M Oliveira Giselle A Oliveira John F Andersen Marcus F Oliveira Pedro L Oliveira Carolina Barillas-Mury |
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Affiliation: | Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America. |
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Abstract: | BackgroundMitochondria perform multiple roles in cell biology, acting as the site of aerobic energy-transducing pathways and as an important source of reactive oxygen species (ROS) that modulate redox metabolism.Methodology/Principal FindingsWe demonstrate that a novel member of the mitochondrial transporter protein family, Anopheles gambiae mitochondrial carrier 1 (AgMC1), is required to maintain mitochondrial membrane potential in mosquito midgut cells and modulates epithelial responses to Plasmodium infection. AgMC1 silencing reduces mitochondrial membrane potential, resulting in increased proton-leak and uncoupling of oxidative phosphorylation. These metabolic changes reduce midgut ROS generation and increase A. gambiae susceptibility to Plasmodium infection.ConclusionWe provide direct experimental evidence indicating that ROS derived from mitochondria can modulate mosquito epithelial responses to Plasmodium infection. |
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